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Calcific Aortic Stenosis is the most common cause of aortic valve disease in developed coun‐ tries. This condition increases in prevalence with the advancing age of the U.S. population, afflicting 2-3 % by age 65 [1]. Aortic valve replacement is the number one indication for sur‐ gical valve replacement in the United States and in Europe. The natural history of severe symptomatic aortic stenosis is associated with 50% mortality within 5 years [2]. Bicuspid aortic valve disease is the most common congenital heart abnormality and it is the most common phenotype of calcific aortic stenosis. The bicuspid aortic valve (BAV) is the most common congenital cardiac anomaly, having a prevalence of 0.9 to 1.37% in the general pop‐ ulation [3]. Understanding the cellular mechanisms of tricuspid versus bicuspid aortic valve lesions will provide further understanding the mechanisms of this disease. Currently, there are three fundamental mechanisms defined in the development of aortic valve disease: 1) oxidative stress via traditional cardiovascular risk factors [4-8,6, 7, 9-12], 2) cellular prolifera‐ tion [13] and 3) osteoblastogenesis in the end stage disease process [14, 15]. Previously, the Wnt/Lrp5 signaling pathway has been identified as a signaling mechanism for cardiovascu‐ lar calcification [5, 16, 17]. The corollaries necessary to define a tissue stem cell niche: 1) physical architecture of the endothelial cells signaling to the adjacent subendothelial cells: the valve interstitial cell along the valve fibrosa. 2) defining the oxidative-mechanical stress gradient necessary to activate Wnt3a/Lrp5 in this tissue stem niche to induce disease. Re‐ cently, the mechanisms of oxidative stress have been identified in the development of calcif‐ ic aortic valve disease. This chapter will outline the factors important in the role of calcific aortic valve disease.

Role of Oxidative Stress in Calcific Aortic Valve Disease: From Bench to Bedside - The Role of a Stem Cell Niche